SOD1 and amyotrophic lateral sclerosis: However, the general contribution of intrinsic hyperexcitability to ALS has been further challenged by studies where data from other iPSC‐derived motor neuron models of ALS 38, 53 and the mutant SOD1 mouse 5, 13, 35 identify intrinsic hypoexcitability rather than hyperexcitability as the key physiological phenotype.